This project addresses the hypothesis that persistent allergic inflammation of the airway enhances the epithelial response to rhinovirus infection, leading to increased synthesis of chemokines, recruitment and activation of lymphocytes and leukocytes, and ultimately bronchial hyperresponsiveness. This would explain the clinical observation that rhinovirus upper respiratory infections exacerbate asthma. The specific aims are 1) to determine the impact of pre-existing allergic imflammation on chemokine synthesis and viral load following experimental rhinovirus 16 (RV16) infection in patients; 2) in vitro stimulation of cultured human primary airway epithelial cells with inflammatory stimuli followed by culture with RV16; and 3) a molecular study of induction of transcription activation factors by RV16 infection.